{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13(1)"],"submitter":["Wu N"],"pubmed_abstract":["The clinical significance of necroptosis in gastric cancer (GC) has yet to be fully elucidated. The purpose of our study was to identify a necroptosis-relevant gene and to establish a prediction model to estimate the prognosis and therapeutic potential in GC. Here, we explored the expression profile of 76 necroptosis-related genes in TCGA-STAD patients. A six-gene risk score prediction model was established via regression analysis of the least absolute shrinkage and selection operator (LASSO) and validated in a separate cohort. Patients were separated into low- or high-risk groups according to the median risk score. We then compared and analyzed the biological process characteristics of two risk groups. Additionally, cell-to-cell communications and metabolic activity were analyzed in a single-cell solution. The in vitro experiments were conducted to explore the biological functions and drug sensitivity of necroptosis-related genes in gastric cancer. Our results identified that compared with the low-risk group, the high-risk group was associated with a higher clinical stage or grade and a worse prognosis. In addition, the low-risk group had higher levels of immunity and immune cell infiltration. Necroptosis was triggered by the TNF pathway in myeloid cells and the glycolysis pathway was altered. Necroptosis-related genes modulated the cell function, including proliferation and migration in vitro. Furthermore, the potential drugs' sensitivity was higher in the low-risk subgroup. These findings could facilitate a better understanding and improve the treatment potential and prognosis of GC patients."],"journal":["Biomolecules"],"pagination":["101"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9856014"],"repository":["biostudies-literature"],"pubmed_title":["Necroptosis Related Genes Predict Prognosis and Therapeutic Potential in Gastric Cancer."],"pmcid":["PMC9856014"],"pubmed_authors":["Yu L","Huang Y","Wu N","Zhang Y","Liu B","Su X","Liu F"],"additional_accession":[]},"is_claimable":false,"name":"Necroptosis Related Genes Predict Prognosis and Therapeutic Potential in Gastric Cancer.","description":"The clinical significance of necroptosis in gastric cancer (GC) has yet to be fully elucidated. The purpose of our study was to identify a necroptosis-relevant gene and to establish a prediction model to estimate the prognosis and therapeutic potential in GC. Here, we explored the expression profile of 76 necroptosis-related genes in TCGA-STAD patients. A six-gene risk score prediction model was established via regression analysis of the least absolute shrinkage and selection operator (LASSO) and validated in a separate cohort. Patients were separated into low- or high-risk groups according to the median risk score. We then compared and analyzed the biological process characteristics of two risk groups. Additionally, cell-to-cell communications and metabolic activity were analyzed in a single-cell solution. The in vitro experiments were conducted to explore the biological functions and drug sensitivity of necroptosis-related genes in gastric cancer. Our results identified that compared with the low-risk group, the high-risk group was associated with a higher clinical stage or grade and a worse prognosis. In addition, the low-risk group had higher levels of immunity and immune cell infiltration. Necroptosis was triggered by the TNF pathway in myeloid cells and the glycolysis pathway was altered. Necroptosis-related genes modulated the cell function, including proliferation and migration in vitro. Furthermore, the potential drugs' sensitivity was higher in the low-risk subgroup. These findings could facilitate a better understanding and improve the treatment potential and prognosis of GC patients.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-22T09:06:55.143Z","creation":"2025-04-05T22:50:31.786Z"},"accession":"S-EPMC9856014","cross_references":{"pubmed":["36671486"],"doi":["10.3390/biom13010101"]}}